Left ventricular distension and venting strategies for patients on venoarterial extracorporeal membrane oxygenation

Abstract

Venoarterial extracorporeal membrane oxygenation (VA ECMO) is an established method of short-term mechanical support for patients in cardiogenic shock, but can create left ventricular (LV) distension. This paper analyzes the physiologic basis of this phenomenon and treatment methods. This is a retrospective review of the existing literature on VA ECMO and LV distension. We undertook a PubMed review of all peer-reviewed papers focusing on VA ECMO, LV distension, and LV venting. We reviewed these papers and synthesized our findings. We also will discuss the various methods of LV venting and venting strategies we use at Columbia. LV distension is becoming an increasingly appreciated aspect of caring for patients on VA ECMO support. The literature demonstrates that the consequences of failing to anticipate, recognize, and treat LV distension are grave, and will worsen an already distended and hypocontractile LV. Myocardial recovery will be hindered, and LV thrombus formation more likely. Early recognition and aggressive management of LV distension is paramount in helping care for this critically ill patient population.

Left Ventricle Unloading with Veno-Arterial Extracorporeal Membrane Oxygenation for Cardiogenic Shock. Systematic Review and Meta-Analysis

“…Several LV unloading strategies have been described and proposed in order to minimize the risk of these complications [14], however, the available evidences are still conflicting whether these techniques are safe and useful adjuncts to VA-ECMO in patients with cardiogenic shock [15][16][17][18].…”

Efficacy of left ventricular unloading strategies during venoarterial extracorporeal membrane oxygenation in patients with cardiogenic shock: a protocol for a systematic review and Bayesian network meta-analysis

“…This NMA may have some limitations. Although LV overload has been reported in many studies, there are still no standardized diagnostic criteria for LV overload and no guidelines for the timing of intervention for it [12,28]. We will not limit the time for LV unloading, so, the time of the intervention of LV overload in different clinical studies maybe not uni ed absolutely.…”

“…Despite the common comparator is VA-ECMO alone, any LV unloading technique adjunct to VA-ECMO could be intervention or comparator in pairwise and network meta-analyses. The network of all possible pairwise comparisons among the eligible interventions is shown in Fig 1. As the surgical techniques of LV venting could be achieved by many approaches, we de ne the surgical LV unloading strategy as follows: (1) implanting LV venting cannulation of the ventricle apex or through the mitral valve from the left atrium (LA); (2) implanting a catheter across the aortic valve percutaneously; (3) implanting LV venting surgical cannulation through the right superior pulmonary vein, LA roof or interatrial groove into LA; (4) transseptal LA cannula; (5) an interatrial septostomy (septostomy usually with ballooning or stent); (6) the surgical or percutaneous pulmonary artery cannulation; (7) simultaneous left and right atrial drainage with the multistage cannula coming from the femoral vein and positioned transeptally [12,17,28,31].…”

“…VA-ECMO works relying on generating varying degrees of retrograde aortic ow, which will increase afterload in the aorta. The increased LV afterload could cause an increase in wall stress and oxygen demand, exacerbate myocardial ischemia, and delaying recovery from CS [12,13]. Elevated LV pressure could further promote LV dilatation, trigger ventricular arrhythmias, and result in elevated left atrial (LA) pressure causing pulmonary edema [14].…”

Hematologic concerns in extracorporeal membrane oxygenation

“…When considering ECMO complications, it is important to acknowledge that many of the patients have multiorgan disease. Patients with dysfunction of the left ventricle are at risk of losing myocardial ejection after VA ECMO initiation due to increased systemic afterload, leading to stasis within the ventricle and aortic root 20‐22 . Many will have inflammatory states from sepsis or other disease processes, which will change both their hematologic laboratory parameters and their overall clotting and bleeding risk.…”